Pharmacology Mnemonics - Flash Cards

Name: Zolpidem (Ambien)

Class: Antianxiety-Sedative-Hypnotic Agent

Mechanism: Binds to BDZ receptors, although it’s not structurally related to BDZs.

Absorption:

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Tolerance and physical dependence rarely develop.

Utility: Short-term treatment of insomnia. As effective as BZDs in prolonging total sleep time and shortening sleep latency. Little effect on sleep stages.

Special Features:

Name: Chloral hydrate

Class: Antianxiety-Sedative-Hypnotic Agent

Mechanism: Sim. to barbiturates

Absorption:

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s:

Utility: Used in hospitals, nursing homes, pediatric dental settings. Mickey Finn.

Special Features: Rarely used.

Name: Pentobarbital

Class: Antianxiety-Sedative-Hypnotic Agent (Barbiturate)

Mechanism: Potentiates GABA transmission by interacting w/GABA receptor. High doses ® direct activation of Cl^- channel ® global CNS synaptic depression.

Absorption:

Dist.:

Metabolism.: Hepatic Metabolism ® inactive Metabolismolites. Signif. induction of hepatic microsomal enzymes ® ­ potential for drug interactions.

Excretion, t½:

Toxicity/S.E.s: Dose-dependent depression of CNS fxn (mild sedation ® sleep ® coma ® coma w/resp. depression ® death). Chronic use of doses 2x-4x hypnotic dosage ® tolerance & psych/phys. dependence. W/drawal symptoms include grand mal seizures and DTs and are potentially lethal.

Utility: Rarely used as backup to other sedative-hypnotic drugs. Suicide.

Special Features: Short-acting agent

Name: Phenobarbital

Class: Antianxiety-Sedative-Hypnotic Agent (Barbiturate) (Antiepileptic:Tonic-Clonic)

Mechanism: Potentiates GABA transmission by interacting w/GABA receptor ® ­ duration of channel opening. High doses ® direct activation of Cl^- channel ® global CNS synaptic depression & block of sustained high freq. repetitive firing..

Absorption:

Dist.: 40-60% protein binding.

Metabolism.: Hepatic Metabolism ® inactive Metabolismolites. Signif. induction of hepatic microsomal enzymes ® ­ potential for drug interactions.

Excretion, t½: 46-136 hr (adults), 37-173 hr (kids).

Toxicity/S.E.s: Dose-dependent depression of CNS fxn (mild sedation ® sleep ® coma ® coma w/resp. depression ® death), cognitive impairment, hyperactivity, ataxia, changes in sleep patterns. Non-dose-rel.—lethargy, ¯ attention span, osteopenia. Idiosync.—allergic dermatitis, Stevens Johnson synd., serum sickness rxn, granulocyte suppress. Chronic use of doses 2x-4x hypnotic dosage ® tolerance & psych/phys. dependence. W/drawal symptoms include grand mal seizures and DTs and are potentially lethal.

Utility: Alt. treatment for gen. tonic-clonic & partial seizures. Alt. treatment of status epilepticus. Rarely used as backup to other sedative-hypnotic drugs. Suicide.

Special Features: Long-acting agent

Name: Flurazepam (Dalmane)

Class: Antianxiety-Sedative-Hypnotic Agent (Benzodiazepine)

Mechanism: Acts on BZD receptors closely coupled to GABA_A receptors ® enhancement of GABA inhib. action via ­ freq. of Cl^- channel opening.

Absorption: Oral ® rapid absorption (large variability in indiv. responsiveness).

Dist.: Protein binding ³50%. CNS.

Metabolism.: Liver microsomal N-dealkylation/hydroxylation, then conjug ® inactive glucuronides. No induction of hepatic microsomal enzymes.

Excretion, t½: Urine—mostly Metabolismolized. Long—24-100 hr. Active Metabolismolites.

Toxicity/S.E.s: Acute—excessive depression of CNS fxns (drowsiness, sleep, confusion, disorientation, ataxia, slurred speech, nystagmus, mild amnesia, dementia). May also cause aggression, hyperactivity, delirium, insomnia. Large doses or mixture w/depressants (e.g., EtOH) may cause resp. depression, coma, hallucinations, nightmares, confusion. Chronic—impaired thinking/memory, weight gain/loss. Habituation & physical dependence ® w/drawal syndrome. Abrupt discontinuation ® risk for convulsion (less risk than w/newer BZDs). Metabolism. ¯ in elderly and by cimetidine. Overdose ® serious resp. depression (rarely fatal w/support). ALL BZDs—Use caution w/­ age, pregnancy, EtOH/subst. abuse, depression, driving/dangerous machinery, use of other CNS depressants, narcolepsy, hypersensitivity, chronic use > 1 wk- 1 month (except for epilepsy). Psych & phys dependence.

Utility: Anxiety, insomnia, alcohol w/drawal. Sedation—all BZDs are DOCs for sedation.

Special Features: Older BZD (longer t½, less potency).

Name: Alprazolam (Xanax)

Class: Antianxiety-Sedative-Hypnotic Agent (Benzodiazepine)

Mechanism: Acts on BZD receptors closely coupled to GABA_A receptors ® enhancement of GABA inhib. action via ­ freq. of Cl^- channel opening.

Absorption: Oral ® rapid absorption (large variability in indiv. responsiveness).

Dist.: Protein binding ³50%. CNS.

Metabolism.: Liver microsomal N-dealkylation/hydroxylation, then conjug ® inactive glucuronides. No induction of hepatic microsomal enzymes.

Excretion, t½: Urine—mostly Metabolismolized. Short—12-15 hr. Active Metabolismolites.

Toxicity/S.E.s: Acute—excessive depression of CNS fxns (drowsiness, sleep, confusion, disorientation, ataxia, slurred speech, nystagmus, mild amnesia, dementia). Early morning awakening, rebound insomnia. May also cause aggression, hyperactivity, delirium, insomnia. Large doses or mixture w/depressants (e.g., EtOH) may cause resp. depression, coma, hallucinations, nightmares, confusion. Chronic—impaired thinking/memory, weight gain/loss. Habituation & physical dependence ® w/drawal syndrome. Abrupt discontinuation ® risk for convulsion (greater risk than w/older BZDs). Metabolism. ¯ in elderly and by cimetidine. Overdose ® serious resp. depression (rarely fatal w/support). Psychological and physical dependence.

Utility: Panic/depression. Anxiety, insomnia, alcohol w/drawal. Sedation—all BZDs are DOCs for sedation.

Special Features: Newer BZD (shorter t½, greater potency).

Name: Triazolam (Halcion)

Class: Antianxiety-Sedative-Hypnotic Agent (Benzodiazepine)

Mechanism: Acts on BZD receptors closely coupled to GABA_A receptors ® enhancement of GABA inhib. action via ­ freq. of Cl^- channel opening.

Absorption: Oral ® rapid absorption (large variability in indiv. responsiveness).

Dist.: Protein binding ³50%. CNS.

Metabolism.: Liver microsomal N-dealkylation/hydroxylation, then conjug ® inactive glucuronides. No induction of hepatic microsomal enzymes.

Excretion, t½: Urine—mostly Metabolismolized. Short—3-5 hr. Active Metabolismolites.

Toxicity/S.E.s: Acute—excessive depression of CNS fxns (drowsiness, sleep, confusion, disorientation, ataxia, slurred speech, nystagmus, mild amnesia, dementia). Early morning awakening, rebound insomnia. May also cause aggression, hyperactivity, delirium, insomnia. Large doses or mixture w/depressants (e.g., EtOH) may cause resp. depression, coma, hallucinations, nightmares, confusion. Chronic—impaired thinking/memory, weight gain/loss. Habituation & physical dependence ® w/drawal syndrome. Abrupt discontinuation ® risk for convulsion (greater risk than w/older BZDs). Metabolism. ¯ in elderly and by cimetidine. Overdose ® serious resp. depression (rarely fatal w/support). Psych & phys dependence.

Utility: Insomnia, anxiety, alcohol w/drawal. Sedation—all BZDs are DOCs for sedation.

Special Features: Newer BZD (shorter t½, greater potency).

Name: Diazepam (Valium)

Class: Antianxiety-Sedative-Hypnotic Agent (Benzodiazepine) (Antiepileptic-Status)

Mechanism: Acts on BZD receptors closely coupled to GABA_A receptors ® enhancement of GABA inhib. action via ­ freq. of Cl^- channel opening.

Absorption: Oral ® rapid absorption (large variability in indiv. responsiveness). IV for seizures & conscious sedation, but may cause pain & phlebitis. IM ® poor bioavailability (avoid).

Dist.: Protein binding 99%. High lipid solubility. Rapid CNS dist. Accum. in fat.

Metabolism.: Liver microsomal N-dealkylation/hydroxylation, then conjug ® inactive glucuronides. No induction of hepatic microsomal enzymes.

Excretion, t½: Urine—mostly Metabolismolized. Long—50-150 hr. Active Metabolismolites.

Toxicity/S.E.s: All dose-related. Acute—excessive depression of CNS fxns (drowsiness, sleep, confusion, disorientation, ataxia, slurred speech, nystagmus, mild amnesia, dementia). May also cause aggression, hyperactivity, delirium, insomnia. Large doses or mixture w/depressants (e.g., EtOH) may cause resp. depression, coma, hallucinations, nightmares, confusion. Chronic—impaired thinking/memory, weight gain/loss. May exacerbate depression. Habituation & physical dependence ® w/drawal syndrome. Abrupt discontinuation ® risk for convulsion (but less risk than w/newer BZDs). Symptoms have long latency (5+ days). Metabolism. ¯ in elderly and by cimetidine. Overdose ® serious resp. depression (rarely fatal w/support). Psych & phys depend.

BZDs are DOCs for sedation. Anticonvulsant—a DOC (IV) for status epilepticus or drug-induced seizures. Skeletal muscle relaxation—spasms, tetanus, orthopedic manipulations.